The human heart is a four chambered, muscular organ that provides blood circulation through the body during a cardiac cycle. The four main chambers include the right atria and right ventricle which supplies the pulmonary circulation, and the left atria and left ventricle which supplies oxygenated blood received from the lungs to the remaining body. To insure that blood flows in one direction through the heart, atrioventricular valves (tricuspid and mitral valves) are present between the junctions of the atria and the ventricles, and semi-lunar valves (pulmonary valve and aortic valve) govern the exits of the ventricles leading to the lungs and the rest of the body. These valves contain leaflets or cusps that open and shut in response to blood pressure changes caused by the contraction and relaxation of the heart chambers. The leaflets move apart from each other to open and allow blood to flow downstream of the valve, and coapt to close and prevent backflow or regurgitation in an upstream manner.
Diseases associated with heart valves, such as those caused by damage or a defect, can include stenosis and valvular insufficiency or regurgitation. For example, valvular stenosis causes the valve to become narrowed and hardened which can prevent blood flow to a downstream heart chamber or structure (e.g., aorta) to occur at the proper flow rate and cause the heart to work harder to pump the blood through the diseased valve. Aortic stenosis, for example, can lead to chest pain, fainting, and heart failure. Valvular insufficiency or regurgitation occurs when the valve does not close completely, allowing blood to flow backwards, thereby causing the heart to be less efficient. For example, aortic valvular insufficiency results in blood pooling in the left ventricle which must then expand its normal capacity to accommodate the pooled volume of blood as well as the new blood received in the subsequent cardiac cycle. For this reason the heart muscle must work harder to pump the extra volume of blood which causes strain of the heart muscle over time as well as raises the blood pressure in the heart. A diseased or damaged valve, which can be congenital, age-related, drug-induced, or in some instances, caused by infection, can result in an enlarged, thickened heart that loses elasticity and efficiency. Other symptoms of heart valve diseases, such as stenosis and valvular insufficiency, can include weakness, shortness of breath, dizziness, fainting, palpitations, anemia and edema, and blood clots which can increase the likelihood of stroke or pulmonary embolism. Such symptoms can often be severe enough to be debilitating and/or life threatening.
Surgical strategies for repairing and/or replacing diseased or damaged heart valves can include percutaneously delivering interventional tools and/or prosthetic heart valve devices through catheter-based systems. Before delivering such tools and prosthetic devices, a guidewire may be used to introduce a delivery catheter and subsequently delivered prosthetic devices and/or tools into the proper position (e.g., within the aortic valve). For example, the delivery catheter may be introduced using a surgical cut down or Seldinger access to the femoral artery in the patient's groin. Once a guidewire is properly placed across the targeted heart valve, the delivery catheter may be introduced over the guidewire to the desired position using over-the-wire (“OTW”) or rapid exchange (“RX”) techniques. Spanning or crossing native heart valves, such as the aortic valve, with percutaneously placed guidewires can present numerous challenges due to differing anatomies and etiologies presented by individual patients. The varying shapes, sizes and other features associated with an abnormal or unhealthy aortic valve can make proper alignment of the guidewire difficult, especially in calcified valves which have a narrower opening during systole. In addition to being time consuming, such difficulties can result, in some instances, in cardiac tissue perforation by the guidewire, left bundle branch block and emboli dislodgement of calcium deposits at the aortic valve.